Journal
MODERN RHEUMATOLOGY
Volume 25, Issue 6, Pages 865-870Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/14397595.2015.1030102
Keywords
Activation-induced cytidine deaminase; Interferon-alpha; MicroRNAs; Peripheral blood mononuclear cells; Systemic lupus erythematosus
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Funding
- Grants-in-Aid for Scientific Research [25461405] Funding Source: KAKEN
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Objective. Recent studies on systemic lupus erythematosus (SLE) revealed that microRNAs (miRNAs or miRs) were involved in its pathogenesis. However, only a limited number of miRNAs have been examined. Methods. We performed quantitative real-time reverse transcription-polymerase chain reaction analyses of peripheral blood mononuclear cells (PBMCs) obtained from 31 untreated SLE patients and 31 healthy subjects to examine the expression levels of miR-155, miR-17, and miR-181b, as well as those of activation-induced cytidine deaminase (AID) and interferon-alpha (IFN-alpha) messenger RNAs (mRNAs). We examined the relationship between miR-181b, AID, and IFN-alpha with a luciferase reporter assay. Results. The expression levels of miR-155, miR-17, and miR-181b were significantly lower in SLE patients than those in healthy controls, whereas those of AID and IFN-alpha mRNAs were significantly higher in SLE patients than those in healthy controls. The expression levels of miR-155, miR-17, and miR-181b inversely correlated with those of AID and IFN-alpha mRNAs in SLE patients. The results of the luciferase reporter assay revealed that miR-181b negatively regulated AID and IFN-alpha. Conclusions. The results of the present study demonstrated for the first time that there is a differential expression and inverse correlation between the levels the miR-155, miR-17, and miR-181b and target molecules, AID and IFN-alpha mRNAs, in PBMCs of untreated SLE patients. These alterations may contribute to the pathogenesis of SLE.
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